Polyamines are ubiquitous aliphatic amines found in both prokaryotic and eukaryotic cells.1 The native polyamines, shown as 1-3 in FIG. 1, are essential growth factors and exist mainly as polycations at physiological pH.2 They are biosynthesized within cells and can also be imported into cells via the polyamine transporter (PAT).3 The polyamines have many functions within cells including key roles in cell proliferation (cancer)4 and in the immune response.5 
The role of polyamines in cancer is well established. Certain cancer tissues are unable to synthesize enough polyamines to sustain their growth rate and rely on polyamine import processes to make up the difference.5 Since polyamines are essential for cell growth, it is not surprising that high levels of polyamines are found in rapidly-dividing cells and cancerous tissues. Moreover, the metabolites of polyamines are often found in the urine of cancer patients at higher levels than normal.6 Indeed, N1,N12-diacetylspermine 9 (a byproduct of spermine) has been shown to be excellent tumor marker for colorectal cancer patients.6-9 
Polyamines also play a role in the immune response.5 Macrophages containing high levels of polyamines have significantly reduced phagocytotic ability.10, 11 Indeed, spermine was recently shown to lower the immune response by inhibiting pro-inflammatory gene expression in macrophages activated by H. pylori.5 Bussière et al have suggested that high spermine levels could prevent the antimicrobial effects of nitric oxide (NO) by inhibiting inducible nitric oxide synthase (iNOS) translation in activated macrophages.5 To support this hypothesis, macrophage bacteriocidal activity was enhanced by transfection with a polyamine biosynthesis inhibitor (i.e., ornithine decarboxylase siRNA) and prevented by spermine addition.5 These provocative results identified a “mechanism of immune dysregulation induced by the H. pylori bacterium in which stimulated spermine synthesis by the arginase-ODC pathway inhibits iNOS translation and NO production, leading to persistence of the bacterium and risk for peptic ulcer disease and gastric cancer.”5 
Inappropriate, dysregulated adaptive mucosal immune response to the intestinal bacteria (flora) is also a prerequisite for initiation and progression of the inflammatory process and tissue damage in inflammatory bowel diseases (IBD) like Crohn's disease (CD) and ulcerative colitis (UC). The mechanism of dysregulated adaptive immune response appears to be defective innate mucosal immunity. Abnormal mucosal macrophages are the key reason for defective innate immunity. For example, mutated recognition protein receptors (e.g. NOD-2, TLR-4) have been shown to be the cause of defective macrophage function in some of the CD patients.12, 13 However, the mechanism of defective innate immunity in patients with UC has not been elucidated.